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D-Amino acid oxidase (DAAO) specifically catalyzes the oxidative deamination of neutral and polar D-amino acids and finally yields byproducts of hydrogen peroxide. Our previous work demonstrated that the spinal astroglial DAAO/hydrogen peroxide (H2O2) pathway was involved in the process of pain and morphine antinociceptive tolerance. This study aimed to report mouse strain specificity of DAAO inhibitors on antinociception and explore its possible mechanism. DAAO inhibitors benzoic acid, CBIO, and SUN significantly inhibited formalin-induced tonic pain in Balb/c and Swiss mice, but had no antinociceptive effect in C57 mice. In contrast, morphine and gabapentin inhibited formalin-induced tonic pain by the same degrees among Swiss, Balb/c and C57 mice. Therefore, mouse strain difference in antinociceptive effects was DAAO inhibitors specific. In addition, intrathecal injection of D-serine greatly increased spinal H2O2 levels by 80.0% and 56.9% in Swiss and Balb/c mice respectively, but reduced spinal H2O2 levels by 29.0% in C57 mice. However, there was no remarkable difference in spinal DAAO activities among Swiss, Balb/c and C57 mice. The spinal expression of glutathione (GSH) and glutathione peroxidase (GPx) activity in C57 mice were significantly higher than Swiss and Balb/c mice. Furthermore, the specific GPx inhibitor D-penicillamine distinctly restored SUN antinociception in C57 mice. Our results reported that DAAO inhibitors produced antinociception in a strain-dependent manner in mice and the strain specificity might be associated with the difference in spinal GSH and GPx activity. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is the most common age-related neurodegenerative disorder. Amyloid-b (Ab) and hyper-phosphorylated tau accumulation are accountable for the progressive neuronal loss and cognitive impairments usually observed in AD. Currently, medications for AD offer moderate symptomatic relief but fail to cure the disease; hence development of effective and safe drugs is urgently needed for AD treatment. In this study, we investigated a Chinese medicine (CM) formulation named NeuroDefend (ND), for reducing amyloid b (Ab) and tau pathology in transgenic AD mice models. Regular oral administration of ND improved cognitive function and memory in 3XTg-AD and 5XFAD mice. In addition, ND reduced beta-amyloid precursor protein (APP), APP C-terminal fragments (CTF-b/a), Ab and 4G8 positive Ab burden in 3XTg-AD and 5XFAD mice. Furthermore, ND efficiently reduced the levels of insoluble phospho-tau protein aggregates and AT8 positive phospho tau neuron load in 3XTg-AD mice. Hence, ND could be a promising candidate for the treatment of AD in humans. [ABSTRACT FROM AUTHOR]

Hippocampal neurogenesis plays a critical role in the formation of new neurons during learning and memory development. Attenuation of neurogenesis in the brain is one of the primary causes of dementia in Alzheimer's disease (AD), and, conversely, modulating the process of hippocampal neurogenesis benefit patients with AD. Traditional Chinese medicine (TCM), particularly herbal medicine, has been in use for thousands of years in Asia and many regions of the world for the treatment of cancer, cardiovascular diseases and neurodegenerative diseases. In this review, we summarize the role of neurotrophic factors, signal transducing factors, epigenetic modulators and neurotransmitters in neurogenesis, and we also discuss the functions of several Chinese herbs and their active molecules in activating multiple pathways involved in neurogenesis. TCM herbs target pathways such as Notch, Wnt, Sonic Hedgehog and receptor tyrosine kinase pathway, leading to activation of a signaling cascade that ultimately enhances the transcription of several important genes necessary for neurogenesis. Given these pathway activating effects, the use of TCM herbs could be an effective therapeutic strategy for the treatment of AD. [ABSTRACT FROM AUTHOR]

The development, survival, and reproduction of Liposcelis decolor (Pearman) (Psocoptera: Liposcelididae), an important insect pest of infested stored products, were evaluated at eight constant temperatures (20-37.5°C). Female L. decolor had four nymphal stadia, whereas males only had three nymphal stadia. Between 20 and 37.5°C, the female developmental period from egg to adult varied from 46.2 d at 20°C to 16.1 d at 35°C, and the male developmental period from egg to adult varied from 41.8 d at 20°C to 13.6 d at 35°C. Based on a nonlinear model, the lower temperature developmental thresholds of female from egg, first through fourth stadia, and combined immature stages were estimated at 12.22, 16.08, 10.93, 8.88, 12.64, and 13.02°C, the upper temperature thresholds were 42.11, 39.44, 41.27, 40.92, 39.20, and 40.52°C, respectively, whereas the lower temperature thresholds of males ranged from 11.68 to 15.86°C, and the upper temperature thresholds ranged from 40.19 to 42.04°C. The survival rate from egg to adult was 57.3% at 32.5°C, 38.4 at 20°C, and 19% at 37.5°C, respectively. After emergence, the adult had a preoviposition period that ranged from 6.8 d at 20°C to 2.3 d at 35°C. L. decolor produced the most eggs (130.4) at 32.5°C and the fewest (24.7) at 37.5°C. The population reared at 32.5°C had the highest intrinsic rate of increase (0.0609) compared with the populations reared at seven other constant temperatures. The populations reared at 35 and 37.5°C had type III survivorship pattern, whereas populations reared at other temperatures had type I survivorship curve as determined by a Weibull frequency distribution. The optimal range of temperature for L. decolor population growth was 27.5-35°C. [ABSTRACT FROM AUTHOR]

In the title compound, C24H18F3N3O, the molecule exists in the enamine–keto tautomeric form. The pyrazolone ring makes dihedral angles of 31.8 (2), 45.4 (2) and 71.2 (2)° with the 1-phenyl, aniline and methylene-bound phenyl rings, respectively. An intramolecular N—H...O hydrogen bond helps to stabilize the molecular conformation. [ABSTRACT FROM AUTHOR]